Ovarian clear cell carcinoma sub-typing by ARID1A expression

Jae Yoon Choi, Hyun Ho Han, YoungTae Kim, Joo Hyun Lee, Baek Gil Kim, Suki Kang, Namhoon Cho

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Purpose: Loss of AT-rich DNA-interacting domain 1A (ARID1A) has been identified as a driving mutation of ovarian clear cell carcinoma (O-CCC), a triple-negative ovarian cancer that is intermediary between serous and endometrioid subtypes, in regards to molecular and clinical behaviors. However, about half of O-CCCs still express BAF250a, the protein encoded by ARID1A. Herein, we aimed to identify signatures of ARID1A-positive O-CCC in comparison with its ARID1A-negative counterpart. Materials and Methods: Seventy cases of O-CCC were included in this study. Histologic grades and patterns of primary tumor, molecular marker immunohistochemistry profiles, and clinical outcomes were analyzed. Results: Forty-eight (69%) O-CCCs did not express BAF250a, which were designated as “ARID1A-negative.” The other 22 (31%) OCCCs were designated as “ARID1A-positive.” ARID1A-positive tumors were more likely to be histologically of high grades (41% vs. 10%, p=0.003), ERβ-positive (45% vs. 17%, p=0.011), and less likely to be HNF1β-positive (77% vs. 96%, p=0.016) and E-cadherinpositive (59% vs. 83%, p=0.028) than ARID1A-negative tumors. Patient age, parity, tumor stage were not significantly different in between the two groups. Cancer-specific survival was not significantly different either. Conclusion: We classified O-CCCs according to ARID1A expression status. ARID1A-positive O-CCCs exhibited distinct immunohistochemical features from ARID1A-negative tumors, suggesting a different underlying molecular event during carcinogenesis.

Original languageEnglish
Pages (from-to)59-66
Number of pages8
JournalYonsei medical journal
Volume58
Issue number1
DOIs
Publication statusPublished - 2017 Jan 1

Fingerprint

Carcinoma
DNA
Neoplasms
Tumor Biomarkers
Parity
Ovarian Neoplasms
Carcinogenesis
Immunohistochemistry
Mutation
Survival
Proteins

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Choi, Jae Yoon ; Han, Hyun Ho ; Kim, YoungTae ; Lee, Joo Hyun ; Kim, Baek Gil ; Kang, Suki ; Cho, Namhoon. / Ovarian clear cell carcinoma sub-typing by ARID1A expression. In: Yonsei medical journal. 2017 ; Vol. 58, No. 1. pp. 59-66.
@article{eeb4878cc8fd4e5a815d556fccf53ac0,
title = "Ovarian clear cell carcinoma sub-typing by ARID1A expression",
abstract = "Purpose: Loss of AT-rich DNA-interacting domain 1A (ARID1A) has been identified as a driving mutation of ovarian clear cell carcinoma (O-CCC), a triple-negative ovarian cancer that is intermediary between serous and endometrioid subtypes, in regards to molecular and clinical behaviors. However, about half of O-CCCs still express BAF250a, the protein encoded by ARID1A. Herein, we aimed to identify signatures of ARID1A-positive O-CCC in comparison with its ARID1A-negative counterpart. Materials and Methods: Seventy cases of O-CCC were included in this study. Histologic grades and patterns of primary tumor, molecular marker immunohistochemistry profiles, and clinical outcomes were analyzed. Results: Forty-eight (69{\%}) O-CCCs did not express BAF250a, which were designated as “ARID1A-negative.” The other 22 (31{\%}) OCCCs were designated as “ARID1A-positive.” ARID1A-positive tumors were more likely to be histologically of high grades (41{\%} vs. 10{\%}, p=0.003), ERβ-positive (45{\%} vs. 17{\%}, p=0.011), and less likely to be HNF1β-positive (77{\%} vs. 96{\%}, p=0.016) and E-cadherinpositive (59{\%} vs. 83{\%}, p=0.028) than ARID1A-negative tumors. Patient age, parity, tumor stage were not significantly different in between the two groups. Cancer-specific survival was not significantly different either. Conclusion: We classified O-CCCs according to ARID1A expression status. ARID1A-positive O-CCCs exhibited distinct immunohistochemical features from ARID1A-negative tumors, suggesting a different underlying molecular event during carcinogenesis.",
author = "Choi, {Jae Yoon} and Han, {Hyun Ho} and YoungTae Kim and Lee, {Joo Hyun} and Kim, {Baek Gil} and Suki Kang and Namhoon Cho",
year = "2017",
month = "1",
day = "1",
doi = "10.3349/ymj.2017.58.1.59",
language = "English",
volume = "58",
pages = "59--66",
journal = "Yonsei Medical Journal",
issn = "0513-5796",
publisher = "Yonsei University College of Medicine",
number = "1",

}

Ovarian clear cell carcinoma sub-typing by ARID1A expression. / Choi, Jae Yoon; Han, Hyun Ho; Kim, YoungTae; Lee, Joo Hyun; Kim, Baek Gil; Kang, Suki; Cho, Namhoon.

In: Yonsei medical journal, Vol. 58, No. 1, 01.01.2017, p. 59-66.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Ovarian clear cell carcinoma sub-typing by ARID1A expression

AU - Choi, Jae Yoon

AU - Han, Hyun Ho

AU - Kim, YoungTae

AU - Lee, Joo Hyun

AU - Kim, Baek Gil

AU - Kang, Suki

AU - Cho, Namhoon

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Purpose: Loss of AT-rich DNA-interacting domain 1A (ARID1A) has been identified as a driving mutation of ovarian clear cell carcinoma (O-CCC), a triple-negative ovarian cancer that is intermediary between serous and endometrioid subtypes, in regards to molecular and clinical behaviors. However, about half of O-CCCs still express BAF250a, the protein encoded by ARID1A. Herein, we aimed to identify signatures of ARID1A-positive O-CCC in comparison with its ARID1A-negative counterpart. Materials and Methods: Seventy cases of O-CCC were included in this study. Histologic grades and patterns of primary tumor, molecular marker immunohistochemistry profiles, and clinical outcomes were analyzed. Results: Forty-eight (69%) O-CCCs did not express BAF250a, which were designated as “ARID1A-negative.” The other 22 (31%) OCCCs were designated as “ARID1A-positive.” ARID1A-positive tumors were more likely to be histologically of high grades (41% vs. 10%, p=0.003), ERβ-positive (45% vs. 17%, p=0.011), and less likely to be HNF1β-positive (77% vs. 96%, p=0.016) and E-cadherinpositive (59% vs. 83%, p=0.028) than ARID1A-negative tumors. Patient age, parity, tumor stage were not significantly different in between the two groups. Cancer-specific survival was not significantly different either. Conclusion: We classified O-CCCs according to ARID1A expression status. ARID1A-positive O-CCCs exhibited distinct immunohistochemical features from ARID1A-negative tumors, suggesting a different underlying molecular event during carcinogenesis.

AB - Purpose: Loss of AT-rich DNA-interacting domain 1A (ARID1A) has been identified as a driving mutation of ovarian clear cell carcinoma (O-CCC), a triple-negative ovarian cancer that is intermediary between serous and endometrioid subtypes, in regards to molecular and clinical behaviors. However, about half of O-CCCs still express BAF250a, the protein encoded by ARID1A. Herein, we aimed to identify signatures of ARID1A-positive O-CCC in comparison with its ARID1A-negative counterpart. Materials and Methods: Seventy cases of O-CCC were included in this study. Histologic grades and patterns of primary tumor, molecular marker immunohistochemistry profiles, and clinical outcomes were analyzed. Results: Forty-eight (69%) O-CCCs did not express BAF250a, which were designated as “ARID1A-negative.” The other 22 (31%) OCCCs were designated as “ARID1A-positive.” ARID1A-positive tumors were more likely to be histologically of high grades (41% vs. 10%, p=0.003), ERβ-positive (45% vs. 17%, p=0.011), and less likely to be HNF1β-positive (77% vs. 96%, p=0.016) and E-cadherinpositive (59% vs. 83%, p=0.028) than ARID1A-negative tumors. Patient age, parity, tumor stage were not significantly different in between the two groups. Cancer-specific survival was not significantly different either. Conclusion: We classified O-CCCs according to ARID1A expression status. ARID1A-positive O-CCCs exhibited distinct immunohistochemical features from ARID1A-negative tumors, suggesting a different underlying molecular event during carcinogenesis.

UR - http://www.scopus.com/inward/record.url?scp=84995766524&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84995766524&partnerID=8YFLogxK

U2 - 10.3349/ymj.2017.58.1.59

DO - 10.3349/ymj.2017.58.1.59

M3 - Article

VL - 58

SP - 59

EP - 66

JO - Yonsei Medical Journal

JF - Yonsei Medical Journal

SN - 0513-5796

IS - 1

ER -